The application of double fluorescence to the rapid selection of atypical cervical epithelial cells spread in monolayers

Monolayer spreads of cervical cells were prepared and reacted in sequence with two fluorescent probes. The nuclei were reacted with 4,6-Diamidino-2-phenylindole (DAPI), resulting in white fluorescence of all cell nuclei. Those cells possessing active guanidinobenzoatase (GB) bound the second probe, rhodamine-alpha-N-agmatine (Rh-Agm), resulting in orange cell surface fluorescence. Atypical epithelial cells possessed both active GB and enlarged nuclei; such cells could easily be recognised by their cytological appearance. We illustrate our results in the form of colour prints which are representative of our observations of cells in both normal and abnormal cervical spreads.     

Germline BRCA1 mutations and loss of the wild-type allele in tumors from families with early onset breast and ovarian cancer

The BRCA1 gene on human chromosome 17q21 is responsible for an autosomal dominant syndrome of inherited early onset breast/ovarian cancer. It is estimated that women harboring a germline BRCA1 mutation incur an 85% lifetime risk of breast cancer and a greatly elevated risk of ovarian cancer. The BRCA1 gene has recently been isolated and mutations have been found in the germline of affected individuals in linked families. Previous studies of loss of heterozygosity (LOH) in breast tumors have been carried out on sporadic tumors derived from individuals without known linkage to BRCA1 and on tumors from linked families. Loss of large regions of chromosome 17 has been observed, but these LOH events could not be unequivocally ascribed to BRCA1. We have studied 28 breast and 6 ovarian tumors from families with strong evidence for linkage between breast cancer and genetic markers flanking BRCA1. These tumors were examined for LOH using genetic markers flanking and within BRCA1, including THRA1, D17S856, EDH17B1, EDH17B2, and D17S183. Forty-six percent (16/34) of tumors exhibit LOH which includes BRCA1. In 8 of 16 tumors the parental origin of the deleted allele could be determined by evaluation of haplotypes of associated family members; in 100% of these cases, the wild-type allele was lost. In some of these families germline mutations in BRCA1 have been determined; analyses of tumors with LOH at BRCA1 have revealed that only the disease-related allele of BRCA1 was present. These data strongly support the hypothesis that BRCA1 is a tumor suppressor gene.     

Sensitivity of Mycobacterium fortuitum by the broth microdilution method determining the inhibitory minimal concentration

A study was conducted on 40 Mycobacterium fortuitum strains isolated from symptomatic patients suffering from respiratory diseases and skin lesions. Their susceptibility to different antimicrobial agents was determined by the broth microdilution method, measuring minimal inhibitory concentration. There was sensitivity of the strains to gentamicin and tetracycline as well as resistance to the tuberculostatic drugs used (isoniazid and ethambutol) and cefalotin.     

Esophageal morphology from Linxian, China. Squamous histologic findings in 754 patients

BACKGROUND: Linxian, China, has one of the highest rates of esophageal cancer in the world. Other authors have described high prevalences of histologic esophagitis, atrophy, and dysplasia in Linxian and have suggested that these findings may represent precancerous lesions in this population. In 1987, a new endoscopic survey allowed the authors to make an independent study of esophageal histology in Linxian. METHODS: There were 1567 satisfactory squamous esophageal biopsies available from 754 patients. These biopsies were classified as normal, atrophy, acanthosis, esophagitis, squamous dysplasia, or squamous cancer. RESULTS: Classified by their worst diagnosis, 56.5% of the 754 patients had normal mucosa, 0.0% atrophy, 11.5% acanthosis, 4.6% esophagitis, 22.7% squamous dysplasia, and 4.6% squamous cancer. CONCLUSIONS: The results show a different distribution of esophageal squamous diagnoses than has been reported previously from this population. The authors believe that the major reason for this discrepancy was differences in histologic criteria. In this survey, seemingly small differences in criteria could cause large differences in apparent disease prevalence; this was especially true for esophagitis. By the criteria used in this study, histologic esophagitis and atrophy are uncommon findings in Linxian, raising questions about their significance as precursor lesions of esophageal cancer in this population.     

Cesium and rubidium salts: effects on voluntary intake of ethanol by the rat

The effects of RbCl and CsCl on voluntary intake of ethanol solution by rats preferring ethanol solution 5% (w/w) over water as the drinking fluid was studied as a function of the dose given and the vehicle injected. Administration of RbCl or CsCl, 0.5 mEq/kg/day or 1.5 mEq/kg/day for three consecutive days, did not alter amounts of ethanol consumed. Repeated administration of RbCl or CsCl, 3.0 mEq/kg/day for three days, produced some moderate reduction in ethanol consumption. Simultaneous injection of RbCl (1.5 mEq/kg) and CsCl (1.5 mEq/kg) resulted in greater and profound lasting decrease in ethanol drinking. The later treatment did not alter specific activities of rat liver alcohol- and aldehyde dehydrogenase from saline treated controls. In general, dissolving the chloride salt of the alkali metals in saline resulted in greater effects on ethanol drinking than that determined after identical dose injected with water as the vehicle. The possible mechanism(s) underlying the effects of alkali metal salts used are suggested.